ERS regulates endometrial epithelial cell autophagy through XBP1s-mediated activation of the PI3K/AKT pathway.

Autophagy is a fundamental cellular activity involved in the renewal of cellular components, occurring primarily in cells subjected to physiological remodeling or pathological stimuli. The occurrence of autophagy is closely related to the endoplasmic reticulum (ER), and ER stress (ERS) occurs when ER homeostasis is disrupted. The current study aimed to analyze the molecular mechanisms underlying the effects of ERS on autophagy in goat endometrial epithelial cells (gEECs).

Transcription factor XBP1s promotes endometritis-induced epithelial-mesenchymal transition by targeting MAP3K2, a key gene in the MAPK/ERK pathway.

The epithelial-mesenchymal transition (EMT) is a biological process whereby epithelial cells are transformed into cells with a mesenchymal phenotype. The transcription factor, X-box binding protein 1 splicing variant (XBP1s) is a key regulator of the endoplasmic reticulum stress response (ERS); but the function of XBP1s in the endometritis-induced EMT process remains unclear. Here we found that uterine tissues from goats with endometritis exhibited an EMT phenotype, with a significant decrease in the epithelial cell polarity marker E-cadherin and a significant increase in the mesenchymal markers N-cadherin and vimentin.